English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Deletion of  Mapt , encoding the microtubule‐binding protein Tau, prevents disease in multiple genetic models of hyperexcitability. To investigate whether the effect of Tau depletion is generalizable across multiple sodium channel gene‐linked models of epilepsy, we examined the  Scn1b   −/−   mouse model of Dravet syndrome, and the  Scn8a   N1768D/+   model of Early Infantile Epileptic Encephalopathy. Both models display severe seizures and early mortality. We found no prolongation of survival between  Scn1b   −/−   ,Mapt   +/+  ,  Scn1b   −/−   ,Mapt   +/−,   or  Scn1b   −/−   ,Mapt   −/−   mice or between  Scn8a   N1768D/+   ,Mapt   +/+  ,  Scn8a   N1768D/+   ,Mapt   +/−  , or  Scn8a   N1768D/+   ,Mapt   −/−   mice. Thus, the effect of  Mapt  deletion on mortality in epileptic encephalopathy models is gene specific and provides further mechanistic insight.

Mapt deletion fails to rescue premature lethality in two models of sodium channel epilepsy